Ancient Mouse Fur Discovery with Mighty Implications

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By Fazale Rana – June 26, 2019

“What a mouse! . . . WHAT A MOUSE!”

The narrator’s exclamation became the signature cry each time the superhero Mighty Mouse carried out the most impossible of feats.

A parody of Superman, Mighty Mouse was the 1942 creation of Paul Terry of Terrytoons Studio for 20th Century Fox. Since then, Mighty Mouse has appeared in theatrical shorts and films, Saturday morning cartoons, and comic books.

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Figure 1: Mighty Mouse. Image credit: Wikipedia

Throughout each episode, the characters sing faux arias—mocking opera—with Mighty Mouse belting out, “Here I am to save the day!” each time he flies into action. As you would expect, many of the villains Mighty Mouse battles are cats, with his archnemesis being a feline named Oil Can Harry.

Mouse Fur Discovery

Recently, a team of researchers headed by scientists from the University of Manchester in the UK went to heroic measures to detect pigments in a 3-million-year-old mouse fossil, nicknamed—you guessed it—“mighty mouse.”1 To detect the pigments, the researchers developed a new method that employs Synchrotron Rapid Scanning X-Ray Fluorescence Imaging to map metal distributions in the fossil, which, in turn, correlate with the types of pigments found in the animal’s fur when it was alive.

This work paves the way for paleontologists to develop a better understanding of past life on Earth, with fur pigmentation being unusually important. The color of an animal’s fur has physiological and behavioral importance and can change relatively quickly over the course of geological timescales through microevolutionary mechanisms.

This discovery also carries importance for the science-faith conversation. Some Christians believe that the recovery of soft tissue remnants, such as the pigments that make up fur, call into question the scientific methods used to determine the age of geological formations and the fossil record. This uncertainty opens up the possibility that our planet (and life on Earth) may be only 6,000 years old.

Is the young-earth interpretation of this advance valid? Is it possible for soft tissue materials to survive for millions of years? If so, how?

Detection of 3-Million-Year-Old Pigment

University of Manchester researchers applied their methodology to an exceptionally well-preserved 3-million-year-old fossil specimen (Apodemus atavus) recovered from the Willershausen conservation site in Germany. The specimen was compressed laterally during the fossilization process and is so well-preserved that imprints of its fur are readily visible.

The research team indirectly identified the pigments that at one time colored the fur by mapping the distribution of metals in the fossil specimen. These metals are known to associate with the pigments eumelanin and pheomelanin, the two main forms of melanin. (Eumelanin produces black and brown hues. Pheomelanin imparts fur, skin, and feathers with a light reddish-brown color.) As it turns out, copper ions chemically interact with eumelanin and pheomelanin. On the other hand, zinc (Zn) ions interact exclusively with pheomelanin by binding to sulfur (S) atoms that are part of this pigment’s molecular structure. Zinc doesn’t interact with eumelanin because sulfur is not part of its chemical composition.

The research team mapped the Zn and S distributions of the mighty mouse fossil and concluded that much of the fur was colored with pheomelanin and, therefore, must have been reddish brown. They failed to detect any pigment in the fur coating the animal’s underbelly and feet, leading them to speculate that the mouse had white fur coating its stomach and feet.

What a piece of science! . . . WHAT A PIECE OF SCIENCE!

Soft Tissues and the Scientific Case for a Young Earth

Paleontologists see far-reaching implications for this work. Roy Wogelius, one of the scientists leading the study, hopes that “these results will mean that we can become more confident in reconstructing extinct animals and thereby add another dimension to the study of evolution.”2

Young-earth creationists (YECs) also see far-reaching implications for this study. Many argue that advances such as this one provide compelling evidence that the earth is young and that the fossil record was laid down as a consequence of a recent global flood.

The crux of the YEC argument centers around the survivability of soft tissue materials. According to common wisdom, soft tissue materials should rapidly degrade once the organism dies. If this is the case, then there is no way soft tissue remnants should hang around for thousands of years, let alone millions. The fact that these materials can be recovered from fossil specimens indicates that the preserved organisms must be only a few thousand years old. And if that’s the case, then the methods used to date the fossils cannot be valid.

At first glance, the argument carries some weight. Most people find it hard to envision how soft tissue materials could survive for vast periods of time, given the wide range of mechanisms that drive the degradation of biological materials.

Preservation Mechanisms for Soft Tissues in Fossils

Despite this initial impression, over the last decade or so paleontologists have identified a number of mechanisms that can delay the degradation of soft tissues long enough for them to become entombed within a mineral shell. When this entombment occurs, the degradation process dramatically slows down. In other words, it is a race against time. Can mineral entombment take place before the soft tissue materials fully decompose? If so, then soft tissue remnants can survive for hundreds of millions of years. And any chemical or physical process that can delay the degradation will contribute to soft tissue survival by giving the entombment process time to take place.

In Dinosaur Blood and the Age of the Earth, I describe several mechanisms that likely promote soft tissue survival. I also discuss the molecular features that contribute to soft tissue preservation in fossils. Not all molecules are made equally. Some are fragile and some robust. Two molecular properties that make molecules unusually durable are cross-linking and aromaticity. As it turns out, eumelanin and pheomelanin possess both.

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Figure 2: Chemical Structure of Eumelanin. Image credit: Wikipedia

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Figure 3: Chemical Structure of Pheomelanin. Image credit: Wikipedia

When considering the chemical structures of eumelanin and pheomelanin, it isn’t surprising that these materials persist in the fossil record for millions of years. In fact, researchers have isolated eumelanin from a fossilized cephalopod ink sac that dates to around 160 million years ago.3

It is also worth noting that the mouse specimen was well-preserved, making it even more likely that durable soft-tissue materials would persist in the fossil. And, keep in mind that the research team detected trace amounts of pigments using sophisticated, state-of-the-art chemical instrumentation.

In short, the recovery of trace levels of soft-tissue materials from fossil remains is not surprising. Soft-tissue materials associated with the mighty mouse specimen—and other fossils, for that matter— can’t save the day for the young-earth paradigm, but they find a ready explanation in an old-earth framework.

Resources

Endnotes
  1. Phillip L. Manning et al., “Pheomelanin Pigment Remnants Mapped in Fossils of an Extinct Mammal,” Nature Communications 10, (May 21, 2019): 2250, doi:10.1038/s41467-019-10087-2.
  2. DOE/SLAC National Accelerator Laboratory, “In a First, Researchers Identify Reddish Coloring in an Ancient Fossil,” Science Daily, May 21, 2019, https://www.sciencedaily.com/releases/2019/05/190521075110.htm
  3. Keely Glass et al., “Direct Chemical Evidence for Eumelanin Pigment from the Jurassic Period,” Proceedings of the National Academy of Sciences USA 109, no. 26 (June 26, 2012): 10218–23, doi:10.1073/pnas.1118448109.

Satellite DNA: Critical Constituent of Chromosomes

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By Fazale Rana – June 26, 2019

Let me explain.

Recently, I wound up with a disassembled cabinet in the trunk of my car. Neither my wife Amy nor I could figure out where to put the cabinet in our home and we didn’t want to store it in the garage. The cabinet had all its pieces and was practically new. So, I offered it to a few people, but there were no takers. It seemed that nobody wanted to assemble the cabinet.

Getting Rid of the Junk

After driving around with the cabinet pieces in my trunk for a few days, I channeled my inner Marie Kondo. This cabinet wasn’t giving me any joy by taking up valuable space in the trunk. So, I made a quick detour on my way home from the office and donated the cabinet to a charity.

When I told Amy what I had done, she expressed surprise and a little disappointment. If she had known I was going to donate the cabinet, she would have kept it for its glass doors. In other words, if I hadn’t donated the cabinet, it would have eventually wound up in our garage because it has nice glass doors that Amy thinks she could have repurposed.

There is a point to this story: The cabinet was designed for a purpose and, at one time, it served a useful function. But once it was disassembled and put in the trunk of my car, nobody seemed to want it. Disassembling the cabinet transformed it into junk. And since my wife loves to repurpose things, she saw a use for it. She didn’t perceive the cabinet as junk at all.

The moral of my little story also applies to the genomes of eukaryotic organisms. Specifically, is it time that evolutionary scientists view some kinds of DNA not as junk, but rather as purposeful genetic elements?

Junk in the Genome

Many biologists hold the view that a vast proportion of the genomes of other eukaryotic organisms is junk, just like the disassembled cabinet I temporarily stored in my car. They believe that, like the unwanted cabinet, many of the different types of “junk” DNA in genomes originated from DNA sequences that at one time performed useful functions. But these functional DNA sequences became transformed (like the disassembled cabinet) into nonfunctional elements.

Evolutionary biologists consider the existence of “junk” DNA as one of the most potent pieces of evidence for biological evolution. According to this view, junk DNA results when undirected biochemical processes and random chemical and physical events transform a functional DNA segment into a useless molecular artifact. Junk pieces of DNA remain part of an organism’s genome, persisting from generation to generation as a vestige of evolutionary history.

Evolutionary biologists highlight the fact that, in many instances, identical (or nearly identical) segments of junk DNA appear in a wide range of related organisms. Frequently, the identical junk DNA segments reside in corresponding locations in these genomes—and for many biologists, this feature clearly indicates that these organisms shared a common ancestor. Accordingly, the junk DNA segment arose prior to the time that the organisms diverged from their shared evolutionary ancestor and then persisted in the divergent evolutionary lines.

One challenging question these scientists ask is, Why would a Creator purposely introduce nonfunctional, junk DNA at the exact location in the genomes of different, but seemingly related, organisms?

Satellite DNA

Satellite DNA, which consists of nucleotide sequences that repeat over and over again, is one class of junk DNA. This highly repetitive DNA occurs within the centromeres of chromosomes and also in the chromosomal regions adjacent to centromeres (referred to as pericentromeric regions).

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Figure: Chromosome Structure. Image credit: Shutterstock

Biologists have long regarded satellite DNA as junk because it doesn’t encode any useful information. Satellite DNA sequences vary extensively from organism to organism. For evolutionary biologists, this variability is a sure sign that these DNA sequences can’t be functional. Because if they were, natural selection would have prevented the DNA sequences from changing. On top of that, molecular biologists think that satellite DNA’s highly repetitive nature leads to chromosomal instability, which can result in genetic disorders.

A second challenging question is, Why would a Creator intentionally introduce satellite DNA into the genomes of eukaryotic organisms?

What Was Thought to Be Junk Turns Out to Have Purpose

Recently, a team of biologists from the University of Michigan (UM) adopted a different stance regarding the satellite DNA found in pericentromeric regions of chromosomes. In the same way that my wife Amy saw a use for the cabinet doors, the researchers saw potential use for satellite DNA. According to Yukiko Yamashita, the UM research head, “We were not quite convinced by the idea that this is just genomic junk. If we don’t actively need it, and if not having it would give us an advantage, then evolution probably would have gotten rid of it. But that hasn’t happened.”1

With this mindset—refreshingly atypical for most biologists who view satellite DNA as junk—the UM research team designed a series of experiments to determine the function of pericentromeric satellite DNA.2 Typically, when molecular biologists seek to understand the functional role of a region of DNA, they either alter it or splice it out of the genome. But, because the pericentromeric DNA occupies such a large proportion of chromosomes, neither option was available to the research team. Instead, they made use of a protein found in the fruit fly Drosophila melanogaster, called D1. Previous studies demonstrated that this protein binds to satellite DNA.

The researchers disabled the gene that encodes D1 and discovered that fruit fly germ cells died. They observed that without the D1 protein, the germ cells formed micronuclei. These structures reflect chromosomal instability and they form when a chromosome or a chromosomal fragment becomes dislodged from the nucleus.

The team repeated the study, but this time they used a mouse model system. The mouse genome encodes a protein called HMGA1 that is homologous to the D1 protein in fruit flies. When they damaged the gene encoding HMGA1, the mouse cells also died, forming micronuclei.

As it turns out, both D1 and HMGA1 play a crucial role, ensuring that chromosomes remain bundled in the nucleus. These proteins accomplish this feat by binding to the pericentromeric satellite DNA. Both proteins have multiple binding sites and, therefore, can simultaneously bind to several chromosomes at once. The multiple binding interactions collect chromosomes into a bundle to form an association site called a chromocenter.

The researchers aren’t quite sure how chromocenter formation prevents micronuclei formation, but they speculate that these structures must somehow stabilize the nucleus and the chromosomes housed in its interior. They believe that this functional role is universal among eukaryotic organisms because they observed the same effects in fruit flies and mice.

This study teaches us two additional lessons. One, so-called junk DNA may serve a structural role in the cell. Most molecular biologists are quick to overlook this possibility because they are hyper-focused on the informational role (encoding the instructions to make proteins) DNA plays.

Two, just because regions of the genome readily mutate without consequences doesn’t mean these sequences aren’t serving some kind of functional role. In the case of pericentromeric satellite DNA, the sequences vary from organism to organism. Most molecular biologists assume that because the sequences vary, they must not be functionally important. For if they were, natural selection would have prevented them from changing. But this study demonstrates that DNA sequences can vary—particularly if DNA is playing a structural role—as long as they don’t compromise DNA’s structural utility. In the case of pericentromeric DNA, apparently the nucleotide sequence can vary quite a bit without compromising its capacity to bind chromocenter-forming proteins (such as D1 and HMGA1).

Is the Evolutionary Paradigm the Wrong Framework to Study Genomes?

Scientists who view biology through the lens of the evolutionary paradigm are often quick to conclude that the genomes of organisms reflect the outworking of evolutionary history. Their perspective causes them to see the features of genomes, such as satellite DNA, as little more than the remnants of an unguided evolutionary process. Within this framework, there is no reason to think that any particular DNA sequence element harbors function. In fact, many life scientists regard these “evolutionary vestiges” as junk DNA. This clearly was the case for satellite DNA.

Yet, a growing body of data indicates that virtually every category of so-called junk DNA displays function. In fact, based on the available data, a strong case can be made that most sequence elements in genomes possess functional utility. Based on these insights, and the fact that pericentromeric satellite DNA persists in eukaryotic genomes, the team of researchers assumed that it must be functional. It’s a clear departure from the way most biologists think about genomes.

Based on this study (and others like it), I think it is safe to conclude that we really don’t understand the molecular biology of genomes.

It seems to me that we live in the midst of a revolution in our understanding of genome structure and function. Instead of being a wasteland of evolutionary debris, the architecture and operations of genomes appear to be far more elegant and sophisticated than anyone ever imagined—at least within the confines of the evolutionary paradigm.

This insight also leads me to wonder if we have been using the wrong paradigm all along to think about genome structure and function. I contend that viewing biological systems as the Creator’s handiwork provides a superior framework for promoting scientific advance, particularly when the rationale for the structure and function of a particular biological system is not apparent. Also, in addressing the two challenging questions, if biological systems have been created, then there must be good reasons why these systems are structured and function the way they do. And this expectation drives further study of seemingly nonfunctional, purposeless systems with the full anticipation that their functional roles will eventually be uncovered.

Though committed to an evolutionary interpretation of biology, the UM researchers were rewarded with success when they broke ranks with most evolutionary biologists and assumed junk regions of the genome were functional. Their stance illustrates the power of a creation model approach to biology.

Sadly, most evolutionary biologists are like me when it comes to old furniture. We lack vision and are quick to see it as junk, when in fact a treasure lies in front of us. And, if we let it, this treasure will bring us joy.

Resources

Endnotes
  1. University of Michigan, “Scientists Discover a Role for ‘Junk’ DNA,” ScienceDaily (April 11, 2018), www.sciencedaily.com/releases/2018/04/180411131659.htm.
  2. Madhav Jagannathan, Ryan Cummings, and Yukiko M. Yamashita, “A Conserved Function for Pericentromeric Satellite DNA,” eLife 7 (March 26, 2018): e34122, doi:10.7554/eLife.34122.

Elderly Man Gazing Fondly at His Date in McDonald’s Inspires Thousands of Romantics Online

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May, 2019

A simple moment of intimacy between an elderly man and his fast food date has melted the hearts of thousands of people across social media.

The heartwarming photo was captured by Al Oliver Reyes Alonzo as he was dining at a McDonald’s in the Philippines last week.

While he was eating his meal, Alonzo spotted an older man who was looking at his female companion with the sweetest expression of love and affection.

As the man leaned his head on his folded arms so he could gaze fondly at his date across the table, Alonzo snapped a photo of the exchange and posted it to Facebook.

The translated caption of the photo simply reads: “Even when we are old, I’d still look at you like this.”

Since publishing the photo to social media, it has been shared thousands of times. Some internet users have used it to pledge their own declarations of love towards their romantic partners; others have expressed their longing to one day experience the same look of love from another person.

Regardless, the picture is the sweetest example of how there can still be plenty of golden moments in your golden years.

Frog Choruses Sing Out a Song of Creation

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BY FAZALE RANA – JUNE 12, 2019

My last name, Rana, is Sanskrit in origin, referring to someone who descends from the Thar Ghar aristocracy. Living in Southern California means I don’t often meet Urdu-speaking people who would appreciate the regal heritage connected to my family name. But I do meet a lot of Spanish speakers. And when I introduce myself, I often see raised eyebrows and smiles.

In Spanish, Rana means frog.

My family has learned to embrace our family’s namesake. In fact, when our kids were little, my wife affectionately referred to our five children as ranitas—little frogs.

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Image: Five Ranitas. Image credit: Shutterstock

Our feelings about these cute and colorful amphibians aside, frogs are remarkable creatures. They engage in some fascinating behaviors. Take courtship, as an example. In many frog species, the males croak to attract the attention of females, with each frog species displaying its own distinct call.

Male frogs croak by filling their vocal sacs with air. This allows them to amplify their croaks for up to a mile away. Oftentimes, male frogs in the same vicinity will all croak together, forming a chorus.

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Image: Male Frog Croaking to Attract a Female. Image credit: Shutterstock

As it turns out, female frogs aren’t the only ones who respond to frog croaks.

A research team from Japan has spent a lot of time listening to and analyzing frog choruses with the hopes of understanding the mathematical structure of the sounds that frogs collectively make when they call out to females. Once they had the mathematical model in hand, the researchers discovered that they could use it to improve the efficiency of wireless data transfer systems.1

This work serves as one more example of scientists and engineers applying insights from biology to drive technology advances and breakthroughs. This approach to technology development (called biomimetics and bioinspiration)—exemplified by the impressive work of the Japanese researchers—has significance that extends beyond engineering. It can be used to make the case that a Creator must have played a role in the design and history of life by marshaling support for two distinct arguments for God’s existence:

Frog Choruses: A Cacophony or a Symphony?

Anyone who has spent time near a pond at night certainly knows the ruckus that an army of male frogs can make when each of them is vying for the attention of females.

All the male frogs living near the pond want to attract females to the same breeding site, but, in doing so, each individual also wants to attract females to his specific territory. Field observations indicate that, instead of engaging in a croaking free-for-all (with neighboring frogs trying to outperform one another), the army of frogs engages in a carefully orchestrated acoustical presentation. As a result, male frogs avoid call overlap with neighboring males on a short timescale, while synchronizing their croaks with the other frogs to produce a chorus on a longer timescale.

The frogs avoid call overlap by alternating between silence and croaking, coordinating with neighboring frogs so that when one frog rests, another croaks. This alternating back-and-forth makes it possible for each individual frog to be heard amid the chorus, and it also results in a symphonic chorus of frog croaks.

The Mathematical Structure of Frog Choruses

To dissect the mathematical structure of frog choruses, the research team placed three male Japanese tree frogs into individual mesh cages that were set along a straight line, with a two-foot separation between each cage. The researchers recorded the frog’s croaks using microphones placed by each cage.

They observed that all three frogs alternated their calls, forming a triphasic synchronization. One frog croaked continuously for a brief period of time and then would rest, while the other two frogs took their turn croaking and resting. The researchers determined that the rest breaks for the frogs were important because of the amount of energy it takes the frogs to produce a call.

All three frogs would synchronize the start and stop of their calls to produce a chorus followed by a period of silence. They discovered that the time between choruses varied quite a bit, without rhyme or reason, and was typically much longer than the chorus time. On the other hand, the croaking of each individual lasted for a predictable time duration that was followed immediately by the croaking of a neighboring frog.

By analyzing the acoustical data, the researchers developed a mathematical model to describe the croaking of individual frogs and the collective behavior of the frogs when they belted out a chorus of calls. Their model consisted of both deterministic and stochastic components.

Use of Frog Choruses for Managing Data Traffic

The researchers realized that the mathematical model they developed could be applied to control wireless sensor networks, such as those that make up the internet of things. These networks entail an array of sensor nodes that transmit data packets, delivering them to a gateway node by multi-hop communication, with data packets transmitted from sensor to sensor until it reaches the gate. During transmission, it is critical for the system to avoid the collision of data packets. It is also critical to regulate the overall energy consumption of the system, to avoid wasting valuable energy resources.

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Image: The Internet of Things Made Up of Wireless Sensors. Image credit: Shutterstock

Through simulation studies, the Japanese team demonstrated that the mathematical model inspired by frog choruses averted the collision of data packets in a wireless sensor array, maximized network connectivity, and enhanced efficiency of the array by minimizing power consumption. The researchers conclude, “This study highlights the unique dynamics of frog choruses over multiple time scales and also provides a novel bio-inspired technology.”2

As important as this work may be for inspiring new technologies, as a Christian, I find its real significance in the theological arena.

Frog Choruses and the Argument from Beauty

The grandeur of nature touches the very core of who we are—if we take the time to let it. But, as the work by the Japanese researchers demonstrates, the grandeur we see all around us in nature isn’t confined to what we perceive with our immediate senses. It exists in the underlying mathematical structure of nature. It is nothing short of amazing to think that such exquisite organization and orchestration characterizes frog choruses, so much so that it can inspire sophisticated data management techniques.

From my vantage point, the beauty and mathematical elegance of nature points to the reality of a Creator.

If God created the universe, then it is reasonable to expect it to be a beautiful universe, one that displays an even deeper underlying beauty in the mathematical structure that defines the universe itself and phenomena within the universe. Yet if the universe came into existence through mechanism alone, there isn’t any real reason to think it would display beauty. In other words, the beauty in the world around us signifies the divine.

Furthermore, if the universe originated through uncaused physical mechanisms, there is no reason to think that humans would possess an appreciation for beauty.

A quick survey of the scientific and popular literature highlights the challenge that the origin of our aesthetic sense creates for the evolutionary paradigm.3 Plainly put: evolutionary biologists have no real explanation for the origin of our aesthetic sense. To be clear, evolutionary biologists have posited explanations to account for the genesis of our capacity to appreciate beauty. But after examining these ideas, we walk away with the strong sense that they are not much more than “just-so stories,” lacking any real evidential support.

On the other hand, if human beings are made in God’s image, as Scripture teaches, we should be able to discern and appreciate the universe’s beauty, made by our Creator to reveal his glory and majesty.

Frog Choruses and the Converse Watchmaker Argument

The idea that biological designs—such as the courting behavior of male frogs—can inspire engineering and technology advances is also highly provocative for other reasons. First, it highlights just how remarkable and elegant the designs found throughout the living realm actually are.

I think that the elegance of these designs points to a Creator’s handiwork. It also makes possible a new argument for God’s existence—one I have named the converse Watchmaker argument. (For a detailed discussion, see my essay titled “The Inspirational Design of DNA” in the book Building Bridges.)

The argument can be stated like this:

  • If biological designs are the work of a Creator, then these systems should be so well-designed that they can serve as engineering models for inspiring the development of new technologies.
  • Indeed, this scenario plays out in the engineering discipline of biomimetics.
  • Therefore, it becomes reasonable to think that biological designs are the work of a Creator.

In fact, I will go one step further. Biomimetics and bioinspiration logically arise out of a creation model approach to biology. That designs in nature can be used to inspire engineering makes sense only if these designs arose from an intelligent Mind.

In fact, I will go one step further. Biomimetics and bioinspiration logically arise out of a creation model approach to biology. That designs in nature can be used to inspire engineering makes sense only if these designs arose from an intelligent Mind. The mathematical structure of frog choruses is yet another example of such bioinspiration.

Frogs really are amazing—and regal—creatures. Listening to a frog chorus can connect us to the beauty of the world around us. And it will one day help all of our electronic devices to connect together. And that’s certainly something to sing about.

Resources

Endnotes
  1. Ikkyu Aihara et al., “Mathematical Modelling and Application of Frog Choruses As an Autonomous Distributed Communication System,” Royal Society Open Science 6, no. 1 (January 2, 2019): 181117, doi:10.1098/rsos.181117.
  2. Aihara et al., “Mathematical Modelling and Application.”
  3. For example, see Ferris Jabr, “How Beauty is Making Scientists Rethink Evolution,” The New York Times Magazine, January 9, 2019, https://www.nytimes.com/2019/01/09/magazine/beauty-evolution-animal.html.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/06/12/frog-choruses-sing-out-a-song-of-creation

Why Would God Create a World with Parasites?

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BY FAZALE RANA – JUNE 5, 2019

A being so powerful and so full of knowledge as a God who could create the universe, is to our finite minds omnipotent and omniscient, and it revolts our understanding to suppose that his benevolence is not unbounded, for what advantage can there be in the sufferings of millions of lower animals throughout almost endless time? This very old argument from the existence of suffering against the existence of an intelligent first cause seems to me a strong one; whereas, as just remarked, the presence of much suffering agrees well with the view that all organic beings have been developed through variation and natural selection.1

—Charles Darwin, The Autobiography of Charles Darwin

If God exists and if he is all-powerful, all-knowing, and all-good, why is there so much pain and suffering in the world? This conundrum keeps many skeptics and seekers from the Christian faith and even troubles some Christians.

Perhaps nothing epitomizes the problem of pain and suffering more than the cruelty observed in nature. Indeed, what advantage can there be in the suffering of millions of animals?

Often, the pain and suffering animals experience is accompanied by unimaginable and seemingly unnecessary cruelty.

Take nematodes (roundworms) as an example. There are over 10,000 species of nematodes. Some are free-living. Others are parasitic. Nematode parasites infect humans, animals, plants, and insects, causing untold pain and suffering. But their typical life cycle in insects seems especially cruel.

Nematodes that parasitize insects usually are free-living in their adult form but infest their host in the juvenile stage. The infection begins when the juvenile form of the parasite enters into the insect host, usually through a body opening, such as the mouth or anus. Sometimes the juveniles drill through the insect’s cuticle.

Once inside the host, the juveniles release bacteria that infect and kill the host, liquefying its internal tissues. As long as the supply of host tissue holds out, the juveniles will live within the insect’s body, even reproducing. When the food supply runs out, the nematodes exit the insect and seek out another host.

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Figure 1: An Entomopathogenic Nematode Juvenile. Image credit: Shutterstock

Why would God create a world with parasitism? Could God really be responsible for a world like the one we inhabit? Many skeptics would answer “no” and conclude that God must not exist.

A Christian Response to the Problem of Evil

One way to defend God’s existence and goodness in the face of animal pain and suffering is to posit that there just might be good reasons for God to create the world the way it is. Perhaps what we are quick to label as evil may actually serve a necessary function.

This perspective gains support based on some recent insights into the benefits that insect parasites impart to ecosystems. A research team from the University of Georgia (UGA) recently unearthed one example of the important role played by these parasites.2 These researchers demonstrated that nematode-infected horned passalus beetles (bess beetles) are more effective at breaking down dead logs in the forest than their parasite-free counterparts—and this difference benefits the ecosystem. Here’s how.

The Benefit Parasites Provide to the Ecosystem

The horned passalus lives in decaying logs. The beetles consume wood through a multistep process. After ingesting the wood, these insects excrete it in a partially digested form. The wood excrement becomes colonized by bacteria and fungi and then is later re-consumed by the beetle.

These insects can become infected by a nematode parasite (Chondronema passali). The parasite inhabits the abdominal cavity of the beetle (though not its gastrointestinal tract). When infected, the horned passalus can harbor thousands of individual nematodes.

To study the effect of this parasite on the horned passalus and the forest ecosystem inhabited by the insect, researchers collected 113 individuals from the woods near the UGA campus. They also collected pieces of wood from the logs bearing the beetles.

In the laboratory, they placed each of the beetles in separate containers that also contained pieces of wood. After three months, they discovered that the beetles infected with the nematode parasite processed 15 percent more wood than beetles that were parasite-free. Apparently, the beetles compensate for the nematode infection by consuming more food. One possible reason for the increased wood consumption may be due to the fact that the parasites draw away essential nutrients from the beetle host, requiring the insect to consume more food.

While it isn’t clear if the parasite infestation harms the beetle (infected beetles have reduced mobility and loss of motor function), it is clear that the infestation benefits the ecosystem. These beetles play a key role in breaking down dead logs and returning nutrients to the forest soil. By increasing the beetles’ wood consumption, the nematodes accelerate this process, benefiting the ecosystem’s overall health.

Cody Prouty, one of the project’s researchers, points out “that although the beetle and the nematode have a parasitic relationship, the ecosystem benefits from not only the beetle performing its function, but the parasite increasing the efficiency of the beetle. Over the course of a few years, the parasitized beetles could process many more logs than unparasitized beetles, and lead to an increase of organic matter in soils.”3

This study is not the first to discover benefits parasites impart to ecosystems. Parasites play a role in shaping ecosystem biodiversity and they intertwine with the food web. The researchers close their article this way: “Countering long-standing unpopular views of parasites is certainly challenging, but perhaps evidence like that presented here will be of use in this effort.”4

Such evidence does not “revolt our understanding,” as Darwin might suggest, but instead enhances our insights into the creation and helps counter the challenge of the problem of evil. Even creatures as gruesome as parasites can serve a beneficial purpose in creation and maybe could rightfully be understood as good.

Resources

Endnotes
  1. Charles Darwin, The Autobiography of Charles Darwin: 1809–1882 (New York: W. W. Norton, 1969), 90.
  2. Andrew K. Davis and Cody Prouty, “The Sicker the Better: Nematode-Infected Passalus Beetles Provide Enhanced Ecosystem Services,” Biology Letters 15, no. 5 (2019): 20180842, doi:10.1098/rsbl.2018.0842.
  3. University of Georgia, “Parasites Help Beetle Hosts Function More Effectively,” ScienceDaily (May 1, 2019), https://www.sciencedaily.com/releases/2019/05/190501131435.htm.
  4. Davis and Prouty,“The Sicker the Better,” 3.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/06/05/why-would-god-create-a-world-with-parasites

Biochemical Grammar Communicates the Case for Creation

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BY FAZALE RANA – MAY 29, 2019

As I get older, I find myself forgetting things—a lot. But, thanks to smartphone technology, I have learned how to manage my forgetfulness by using the “Notes” app on my iPhone.

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Figure 1: The Apple Notes app icon. Image credit: Wikipedia

This app makes it easy for me to:

  • Jot down ideas that suddenly come to me
  • List books I want to read and websites I want to visit
  • Make note of musical artists I want to check out
  • Record “to do” and grocery lists
  • Write down details I need to have at my fingertips when I travel
  • List new scientific discoveries with implications for the RTB creation model that I want to blog about, such as the recent discovery of a protein grammar calling attention to the elegant design of biochemical systems

And the list goes on. I will never forget, again!

On top of that, I can use the Notes app to categorize and organize all my notes and house them in a single location. Thus, I don’t have to manage scraps of paper that invariably wind up getting scattered all over the place—and often lost.

And, as a bonus, the Notes app anticipates the next word I am going to use even before I type it. I find myself relying on this feature more and more. It is much easier to select a word than type it out. In fact, the more I use this feature, the better the app becomes at anticipating the next word I want to type.

Recently, a team of bioinformaticists from the University of Alabama, Birmingham (UAB) and the National Institutes of Health (NIH) used the same algorithm the Notes app uses to anticipate word usage to study protein architectures.1 Their analysis reveals new insight into the structural features of proteins and also highlights the analogy between the information housed in these biomolecules and human language. This analogy contributes to the revitalized Watchmaker argument presented in my book The Cell’s Design.

N-Gram Language Modeling

The algorithm used by the Notes app to anticipate the next word the user will likely type is called n-gram language modeling. This algorithm determines the probability of a word being used based on the previous word (or words) typed. (If the probability is based on a single word, it is called a unigram probability. If the calculation is based on the previous two words, it is called a bigram probability, and so on.) This algorithm “trains” the Notes app so that the more I use it, the more reliable the calculated probabilities—and, hence, the better the word recommendations.

N-Gram Language Modeling and the Case for a Creator

To understand why the work of research team from UAB and NIH provides evidence for a Creator’s role in the origin and design of life, a brief review of protein structure is in order.

Protein Structure

Proteins are large complex molecules that play a key role in virtually all of the cell’s operations. Biochemists have long known that the three-dimensional structure of a protein dictates its function.

Because proteins are such large complex molecules, biochemists categorize protein structure into four different levels: primary, secondary, tertiary, and quaternary structures. A protein’s primary structure is the linear sequence of amino acids that make up each of its polypeptide chains.

The secondary structure refers to short-range three-dimensional arrangements of the polypeptide chain’s backbone arising from the interactions between chemical groups that make up its backbone. Three of the most common secondary structures are the random coil, alpha (α) helix, and beta (β) pleated sheet.

Tertiary structure describes the overall shape of the entire polypeptide chain and the location of each of its atoms in three-dimensional space. The structure and spatial orientation of the chemical groups that extend from the protein backbone are also part of the tertiary structure.

Quaternary structure arises when several individual polypeptide chains interact to form a functional protein complex.

 

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Figure 2: The four levels of protein structure. Image credit: Shutterstock

Protein Domains

Within the tertiary structure of proteins, biochemists have discovered compact, self-contained regions that fold independently. These three-dimensional regions of the protein’s structure are called domains. Some proteins consist of a single compact domain, but many proteins possess several domains. In effect, domains can be thought to be the fundamental units of a protein’s tertiary structure. Each domain possesses a unique biochemical function. Biochemists refer to the spatial arrangement of domains as a protein’s domain architecture.

Researchers have discovered several thousand distinct protein domains. Many of these domains recur in different proteins, with each protein’s tertiary structure comprised of a mix-and-match combination of protein domains. Biochemists have also learned that a relationship exists between the complexity of an organism and the number of unique domains found in its set of proteins and the number of multi-domain proteins encoded by its genome.

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Figure 3: Pyruvate kinase, an example of a protein with three domains. Image credit: Wikipedia

The Key Question in Protein Chemistry

As much progress as biochemists have made characterizing protein structure over the last several decades, they still lack a fundamental understanding of the relationship between primary structure (the amino acid sequence) and tertiary structure and, hence, protein function. In order to develop this insight, they need to determine the “rules” that dictate the way proteins fold. Treating proteins as information systems can help determine some of these rules.

Protein as Information Systems

Proteins are not only large, complex molecules but also information-harboring systems. The amino acid sequence that defines a protein’s primary structure is a type of information—biochemical information—with the individual amino acids analogous to the letters that make up an alphabet.

N-Gram Analysis of Proteins

To gain insight into the relationship between a protein’s primary structure and its tertiary structures, the researchers from UAB and NIH carried out an n-gram analysis on the 23 million protein domains found in the protein sets of 4,800 species found across all three domains of life.

These researchers point out that an individual amino acid in a protein’s primary structure doesn’t contain information just as an individual letter in an alphabet doesn’t harbor any meaning. In human language, the most basic unit that conveys meaning is a word. And, in proteins, the most basic unit that conveys biochemical meaning is a domain.

To decipher the “grammar” used by proteins, the researchers treated adjacent pairs of protein domains in the tertiary structure of each protein in the sample set as a bigram (similar to two words together). Surveying the proteins found in their data set of 4,800 species, they discovered that 95% of all the possible domain combinations don’t exist!

This finding is key. It indicates that there are, indeed, rules that dictate the way domains interact. In other words, just like certain word combinations never occur in human languages because of the rules of grammar, there appears to be a protein “grammar” that constrains the domain combinations in proteins. This insight implies that physicochemical constraints (which define protein grammar) dictate a protein’s tertiary structure, preventing 95% of conceivable domain-domain interactions.

Entropy of Protein Grammar

In thermodynamics, entropy is often used as a measure of the disorder of a system. Information theorists borrow the concept of entropy and use it to measure the information content of a system. For information theorists, the entropy of a system is indirectly proportional to the amount of information contained in a sequence of symbols. As the information content increases, the entropy of the sequence decreases, and vice versa. Using this concept, the UAB and NIH researchers calculated the entropy of the protein domain combinations.

In human language, the entropy increases as the vocabulary increases. This makes sense because, as the number of words increases in a language, the likelihood that random word combinations would harbor meaning decreases. In like manner, the research team discovered that the entropy of the protein grammar increases as the number of domains increases. (This increase in entropy likely reflects the physicochemical constraints—the protein grammar, if you will—on domain interactions.)

Human languages all carry the same amount of information. That is to say, they all display the same entropy content. Information theorists interpret this observation as an indication that a universal grammar undergirds all human languages. It is intriguing that the researchers discovered that the protein “languages” across prokaryotes and eukaryotes all display the same level of entropy and, consequently, the same information content. This relationship holds despite the diversity and differences in complexity of the organism in their data set. By analogy, this finding indicates that a universal grammar exists for proteins. Or to put it another way, the same set of physicochemical constraints dictate the way protein domains interact for all organisms.

At this point, the researchers don’t know what the grammatical rules are for proteins, but knowing that they exist paves the way for future studies. It also generates hope that one day biochemists might understand them and, in turn, use them to predict protein structure from amino acid sequences.

This study also illustrates how fruitful it can be to treat biochemical systems as information systems. The researchers conclude that “The similarities between natural languages and genomes are apparent when domains are treated as functional analogs of words in natural languages.”2

In my view, it is this relationship that points to a Creator’s role in the origin and design of life.

Protein Grammar and the Case for a Creator

As discussed in The Cell’s Design, the recognition that biochemical systems are information-based systems has interesting philosophical ramifications. Common, everyday experience teaches that information derives solely from the activity of human beings. So, by analogy, biochemical information systems, too, should come from a divine Mind. Or at least it is rational to hold that view.

But the case for a Creator strengthens when we recognize that it’s not merely the presence of information in biomolecules that contributes to this version of a revitalized Watchmaker analogy. Added vigor comes from the UAB and NIH researchers’ discovery that the mathematical structure of human languages and biochemical languages is identical.

Skeptics often dismiss the updated Watchmaker argument by arguing that biochemical information is not genuine information. Instead, they maintain that when scientists refer to biomolecules as harboring information, they are employing an illustrative analogy—a scientific metaphor—and nothing more. They accuse creationists and intelligent design proponents of misconstruing their use of analogical language to make the case for design.3

But the UAB and NIH scientists’ work questions the validity of this objection. Biochemical information has all of the properties of human language. It really is information, just like the information we conceive and use to communicate.

Is There a Biochemical Anthropic Principle?

This discovery also yields another interesting philosophical implication. It lends support to the existence of a biochemical anthropic principle. Discovery of a protein grammar means that there are physicochemical constraints on protein structure. It is remarkable to think that protein tertiary structures may be fundamentally dictated by the laws of nature, instead of being the outworking of an historically contingent evolutionary history. To put it differently, the discovery of a protein grammar reveals that the structure of biological systems may reflect some deep, underlying principles that arise from the very nature of the universe itself. And yet these structures are precisely the types of structures life needs to exist.

I interpret this “coincidence” as evidence that our universe has been designed for a purpose. And as a Christian, I find that notion to resonate powerfully with the idea that life manifests from an intelligent Agent—namely, God.

Resources to Dig Deeper

Endnotes
  1. Lijia Yu et al., “Grammar of Protein Domain Architectures,” Proceedings of the National Academy of Sciences, USA 116, no. 9 (February 26, 2019): 3636–45, doi:10.1073/pnas.1814684116.
  2. Yu et al., 3636–45.
  3. For example, see Massimo Pigliucci and Maarten Boudry, “Why Machine-Information Metaphors Are Bad for Science and Science Education,” Science and Education 20, no. 5–6 (May 2011): 453–71; doi:10.1007/s11191-010-9267-6.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/05/29/biochemical-grammar-communicates-the-case-for-creation

Why Would God Create a World Where Animals Eat Their Offspring?

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BY FAZALE RANA – MAY 22, 2019

What a book a Devil’s chaplain might write on the clumsy, wasteful, blundering, low and horridly cruel works of nature!

–Charles Darwin, “Letter to J. D. Hooker,” Darwin Correspondence Project

You may not have ever heard of him, but he played an important role in ushering in the Darwinian revolution in biology. His name was Asa Gray.

Gray (1810–1888) was a botanist at Harvard University. He was among the first scientists in the US to adopt Darwin’s theory of evolution. Asa Gray was also a devout Christian.

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Asa Gray in 1864. Image credit: John Adams Whipple, Wikipedia

Gray was convinced that Darwin’s theory of evolution was sound. He was also convinced that nature displayed unmistakable evidence for design. For this reason, he reasoned that God must have used evolution as the means to create and, in doing so, Gray may have been the first person to espouse theistic evolution.

In his book Darwinia, Asa Gray presents a number of essays defending Darwin’s theory. Yet, he also expresses his deepest convictions that nature is filled with indicators of design. He attributed that design to a type of God-ordained, God-guided process. Gray argued that God is the source of all evolutionary change.

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Gray and Darwin struck up a friendship and exchanged around 300 letters. In the midst of their correspondence, Gray asked Darwin if he thought it possible that God used evolution as the means to create. Darwin’s reply revealed that he wasn’t very impressed with this idea.

I cannot persuade myself that a beneficent & omnipotent God would have designedly created the Ichneumonidæ with the express intention of their feeding within the living bodies of caterpillars, or that a cat should play with mice. Not believing this, I see no necessity in the belief that the eye was expressly designed. On the other hand I cannot anyhow be contented to view this wonderful universe & especially the nature of man, & to conclude that everything is the result of brute force. I am inclined to look at everything as resulting from designed laws, with the details, whether good or bad, left to the working out of what we may call chance. Not that this notion at all satisfies me. I feel most deeply that the whole subject is too profound for the human intellect. A dog might as well speculate on the mind of Newton. Let each man hope & believe what he can.1

Darwin could not embrace Gray’s theistic evolution because of the cruelty he saw in nature that seemingly causes untold pain and suffering in animals. Darwin—along with many skeptics today—couldn’t square a world characterized by that much suffering with the existence of a God who is all-powerful, all-knowing, and all-good.

Filial Cannibalism

The widespread occurrence of filial cannibalism (when animals eat their young or consume their eggs after laying them) and abandonment (leading to death) exemplify such cruelty in animals. It seems such a low and brutal feature of nature.

Why would God create animals that eat their offspring and abandon their young?

Is Cruelty in Nature Really Evil?

But what if there are good reasons for God to allow pain and suffering in the animal kingdom? I have written about good scientific reasons to think that a purpose exists for animal pain and suffering (see “Scientists Uncover a Good Purpose for Long-Lasting Pain in Animals” by Fazale Rana).

And, what if animal death is a necessary feature of nature? Other studies indicate that animal death promotes biodiversity and ecosystem stability (see “Of Weevils and Wasps: God’s Good Purpose in Animal Death” by Maureen Moser, and “Animal Death Prevents Ecological Meltdown” by Fazale Rana).

There also appears to be a reason for filial cannibalism and offspring abandonment, at least based on a study by researchers from Oxford University (UK) and the University of Tennessee.2 These researchers demonstrated that filial cannibalism and offspring abandonment comprise a form of parental care.

What? How is that conclusion possible?

It turns out that when animals eat their offspring or abandon their young, the reduction promotes the survival of the remaining offspring. To arrive at this conclusion, the researchers performed mathematical modeling of a generic egg-laying species. They discovered that when animals sacrificed a few of their young, the culling led to greater fitness for their offspring than when animals did not engage in filial cannibalism or egg abandonment.

These behaviors become important when animals lay too many eggs. In order to properly care for their eggs (protect, incubate, feed, and clean), animals confine egg-laying to a relatively small space. This practice leads to a high density of eggs. But this high density can have drawbacks, making the offspring more vulnerable to diseases and lack of sufficient food and oxygen. Filial cannibalism reduces the density, ensuring a greater chance of survival for those eggs that are left behind. So, ironically, when egg density is too high for the environmental conditions, more offspring survive when the parents consume some, rather than none, of the eggs.

So, why lay so many eggs in the first place?

In general, the more eggs that are laid, the greater the number of surviving offspring—assuming there are unlimited resources and no threats of disease. But it is difficult for animals to know how many eggs to lay because the environment is unpredictable and constantly changing. A better way to ensure reproductive fitness is to lay more eggs and remove some of them if the environment can’t sustain the egg density.

So, it appears as if there is a good reason for God to create animals that eat their young. In fact, you might even argue that filial cannibalism leads to a world with less cruelty and suffering than a world where filial cannibalism doesn’t exist at all. This feature of nature is consistent with the idea of an all-powerful, all-knowing, and all-good God who has designed the creation for his good purposes.

Resources

Endnotes
  1. To Asa Gray 22 May [1860],” Darwin Correspondence Project, University of Cambridge, accessed May 15, 2019, https://www.darwinproject.ac.uk/letter/DCP-LETT-2814.xml.
  2. Mackenzie E. Davenport, Michael B. Bansall, and Hope Klug, “Unconventional Care: Offspring Abandonment and Filial Cannibalism Can Function as Forms of Parental Care,” Frontiers in Ecology and Evolution 7 (April 17, 2019): 113, doi:10.3389/fevo.2019.00113.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/05/22/why-would-god-create-a-world-where-animals-eat-their-offspring

Competitive Endogenous RNA Hypothesis Supports the Case for Creation

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BY FAZALE RANA – MAY 15, 2019

When Francis Crick, codiscoverer of the DNA double helix, first conceived of molecular biology’s organizing principle in 1958, he dubbed it the central dogma. He soon came to regret the term. In his autobiographical account, What Mad Pursuit, Crick writes:

I called this idea the central dogma, for two reasons, I suspect. I had already used the obvious word hypothesis in the sequence hypothesis, and in addition I wanted to suggest that this new assumption was more central and more powerful….As it turned out, the use of the word dogma caused almost more trouble than it was worth. Many years later Jacques Monod pointed out to me that I did not appear to understand the correct use of the word dogma, which is a belief that cannot be doubted. I did apprehend this in a vague sort of way but since I thought that all religious beliefs were without foundation, I used the word the way I myself thought about it, not as most of the world does, and simply applied it to a grand hypothesis that, however plausible, had little direct experimental support.1

Even though Crick rued labeling his idea as “dogma,” the term seems to fit, all the connotations aside, because of its singular importance to molecular biology.

The Central Dogma of Molecular Biology

The central dogma of molecular biology describes the directional flow of information in the cell, which moves from DNA to RNA to proteins. Information can flow from DNA to DNA during DNA replication, from DNA to RNA during transcription, and from RNA back to DNA during reverse transcription. However, biochemical information can’t flow from proteins to either RNA or DNA.

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Figure 1: The Central Dogma of Molecular Biology. Image credit: Shutterstock

Is There a New Dogma in Molecular Biology?

In my opinion as a biochemist, if there is an idea that has the potential to rival the significance of the central dogma, it just might be the competitive endogenous RNA (ceRNA) hypothesis. This newer model provides a comprehensive description of the role messenger RNA (mRNA) molecules play in regulating gene expression, thereby influencing the flow of information from DNA to proteins.

The ceRNA hypothesis also provides an elegant rationale for why the genomes of eukaryotic organisms contain pseudogenes (including unitary pseudogenes) and encode long noncoding RNA molecules. Additionally, it explains why duplicated pseudogenes resemble corresponding intact genes. In doing all this, the ceRNA hypothesis provides support for the RTB’s genomics model—which interprets the structure and activities associated with genomes from a creation or design standpoint. (An overview of the RTB genomics model can be found in the updated and expanded 2nd edition of Who Was Adam?)

The Competitive Endogenous RNA Hypothesis

I discuss the ceRNA hypothesis in a previous article. So, I’ll offer just a brief description here. According to the central dogma, the final step in the flow of biochemical information is the production of proteins at the ribosome, directed by the information housed in mRNA. Biochemists have discovered an elaborate mechanism that selectively degrades mRNA transcripts before they can reach this point. This degradation process controls gene expression by dictating the amount of protein produced.

Molecules called microRNAs bind to the mRNA’s 3′ untranslated region, which flags the transcript for destruction by RNA-induced silencing complex (RISC). A number of distinct microRNA species exist in the cell. Each microRNA species bind to specific sites in the 3′ untranslated region of mRNA transcripts. (These binding locations are called microRNA response elements or MREs.)

A network of genes shares the same set of MREs and, consequently, will bind to the same set of microRNAs. When one gene is transcribed, it will influence the expression of all the other genes in its network. And when one gene in the network becomes up-regulated (leading to increased transcription of that gene), the expression of all the genes in the network increases. Why? Because the increased level of that particular transcript exerts a “sponge effect” that consumes more of the microRNAs that would otherwise target other transcripts for degradation.

The Competitive Endogenous RNA Hypothesis and the Role of Junk DNA

The ceRNA hypothesis elegantly explains the functional utility of three classes of junk DNA: duplicated and unitary pseudogenes, plus long noncoding RNAs. As it turns out, the transcripts produced from these types of so-called junk DNA also harbor MREs. None of these transcripts codes for proteins yet they play an indispensable role in regulating gene expression. In fact, all three are much better suited for the role of molecular sponges precisely because they aren’t translated into proteins.

Of particular utility are duplicated pseudogenes due to their close structural resemblance to the corresponding coding genes. Duplicated pseudogenes not only exert a sponge effect but also serve as decoys that allow the transcripts of the intact genes to escape degradation and to be translated into proteins.

Is the Competitive Endogenous RNA Hypothesis Valid?

This question has generated a minor scientific controversy. Some studies provide experimental support for this idea while others question the physiological relevance of ceRNAs. In light of this debate, a team of researchers headed by investigators from Columbia University sought to validate this hypothesis on a large-scale.They discovered that ceRNA interactions can disrupt the expression of thousands of genes. The team concluded that “ceRNA regulation is the norm not the exception…and that ceRNA interactions have genome-wide effects on gene expression.”3

These researchers think that this insight sheds light on tumor biology because dysregulation of ceRNAs have been implicated in some cancers. Their work also has theological significance because it undermines one of the most significant challenges to design arguments and, in turn, can be marshaled in support of the RTB genomics model.

The Competitive Endogenous Hypothesis and the Case for a Creator

Evolutionary biologists have long maintained that identical (or nearly identical) junk DNA sequences (such as pseudogene sequences) found in corresponding locations in genomes of organisms that naturally cluster together (such as humans and the great apes) provide compelling evidence that these organisms must have evolved from a shared ancestor. This interpretation was compelling because junk DNA sequences seemed to be useless vestiges of evolutionary history.

Creationists and intelligent design proponents had little to offer by way of evidence for the intentional design of genomes. But research in recent years has revealed that virtually every class of junk DNA has function. It seems, then, that shared junk DNA sequences can be understood as shared designs, which is what the RTB genomics model predicts.

Additionally, the ceRNA hypothesis supports the RTB genomics even further. This hypothesis provides an elegant explanation for the widespread existence of pseudogenes in genomes and their structural similarity to intact genes.

Could it be that the idea of religious dogma affirming a Creator’s role in life’s design and history has merit?

Resources

Endnotes
  1. Francis Crick, What Mad Pursuit (New York: Basic Books, 1988), 109.
  2. Hua-Sheng Chiu et al., “High-Throughput Validation of ceRNA Regulatory Networks,” BMC Genomics 18 (2017): 418, doi:10.1186/s12864-017-3790-7.
  3. Chiu et al., 418.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/05/15/competitive-endogenous-rna-hypothesis-supports-the-case-for-creation

Pseudogene Discovery Pains Evolutionary Paradigm

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BY FAZALE RANA – MAY 8, 2019

It was one of the most painful experiences I ever had. A few years ago, I had two back-to-back bouts of kidney stones. I remember it as if it were yesterday. Man, did it hurt when I passed the stones! All I wanted was for the emergency room nurse to keep the Demerol coming.

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Figure 1: Schematic Depiction of Kidney Stones Moving through the Urinary Tract. Image Credit: Shutterstock

When all that misery was going down, I wished I was one of those rare individuals who doesn’t experience pain. There are some people who, due to genetic mutations, live pain-free lives. This condition is called hypoalgesia. (Of course, there is a serious downside to hypoalgesia. Pain lets us know when our body is hurt or sick. Because hypoalgesics can’t experience pain, they are prone to serious injury, etc.)

Biomedical researchers possess a keen interest in studying people with hypoalgesia. Identifying the mutations responsible for this genetic condition helps investigators understand the physiological processes that undergird the pain sensation. This insight then becomes indispensable to guiding efforts to develop new drugs and techniques to treat pain.

By studying the genetic profile of a 66-year-old woman who lived a lifetime with pain-free injuries, a research team from the UK recently discovered a novel genetic mutation that causes hypoalgesia.1 The mutation responsible for this patient’s hypoalgesia occurred in a pseudogene, a region of the genome considered nonfunctional “junk DNA.”

This discovery adds to the mounting evidence that shows junk DNA is functional. At this point, molecular geneticists have demonstrated that virtually every class of junk DNA has function. This notion undermines the best evidence for common descent and, hence, undermines an evolutionary interpretation of biology. More importantly, the discovery adds support for the competitive endogenous RNA hypothesis, which can be marshaled to support RTB’s genomics model. It is becoming more and more evident to me that genome structure and function reflect the handiwork of a Creator.

The Role of a Pseudogene in Mediating Hypoalgesia

To identify the genetic mutation responsible for the 66-year-old’s hypoalgesia, the research team scanned her DNA along with samples taken from her mother and two children. The team discovered two genetic changes: (1) mutations to the FAAH gene that reduced its expression, and (2) deletion of part of the FAAH pseudogene.

The FAAH gene encodes for a protein called fatty acid amide hydrolase (FAAH). This protein breaks down fatty acid amides. Some of these compounds interact with cannabinoid receptors. These receptors are located in the membranes of cells found in tissues throughout the body. They mediate pain sensation, among other things. When fatty acid amide concentrations become elevated in the circulatory system, it produces an analgesic effect.

Researchers found elevated fatty acid amide levels in the patient’s blood, consistent with reduced expression of the FAAH gene. It appears that both mutations are required for the complete hypoalgesia observed in the patient. The patient’s mother, daughter, and son all display only partial hypoalgesia. The mother and daughter have the same mutation in the FAAH gene but an intact FAAH pseudogene. The patient’s son is missing the FAAH pseudogene, but has a “normal” FAAH gene.

Based on the data, it looks like proper expression levels of the FAAH gene require an intact FAAH pseudogene. This is not the first time that biomedical researchers have observed the same effect. There are a number of gene-pseudogene pairs in which both must be intact and transcribed for the gene to be expressed properly. In 2011, researchers from Harvard University proposed that the competitive endogenous RNA hypothesis explains why transcribed pseudogenes are so important for gene expression.2

The Competitive Endogenous RNA Hypothesis

Biochemists and molecular biologists have long believed that the primary mechanism for regulating gene expression centered around controlling the frequency and amount of mRNA produced during transcription. For housekeeping genes, mRNA is produced continually, while for genes that specify situational proteins, it is produced as needed. Greater amounts of mRNA are produced for genes expressed at high levels and limited amounts for genes expressed at low levels.

Researchers long thought that once the mRNA was produced it would be translated into proteins, but recent discoveries indicate this is not the case. Instead, an elaborate mechanism exists that selectively degrades mRNA transcripts before they can be used to direct the protein production at the ribosome. This mechanism dictates the amount of protein produced by permitting or preventing mRNA from being translated. The selective degradation of mRNA also plays a role in gene expression, functioning in a complementary manner to the transcriptional control of gene expression.

Another class of RNA molecules, called microRNAs, mediates the selective degradation of mRNA. In the early 2000s, biochemists recognized that by binding to mRNA (in the 3′ untranslated region of the transcript), microRNAs play a crucial role in gene regulation. Through binding, microRNAs flag the mRNA for destruction by RNA-induced silencing complex (RISC).

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Figure 2: Schematic of the RNA-Induced Silencing Mechanism. Image Credit: Wikipedia

Various distinct microRNA species in the cell bind to specific sites in the 3′ untranslated region of mRNA transcripts. (These binding locations are called microRNA response elements.) The selective binding by the population of microRNAs explains the role that duplicated pseudogenes play in regulating gene expression.

The sequence similarity between the duplicated pseudogene and the corresponding “intact” gene means that the same microRNAs will bind to both mRNA transcripts. (It is interesting to note that most duplicated pseudogenes are transcribed.) When microRNAs bind to the transcript of the duplicated pseudogene, it allows the transcript of the “intact” gene to escape degradation. In other words, the transcript of the duplicated pseudogene is a decoy. The mRNA transcript can then be translated and, hence, the “intact” gene expressed.

It is not just “intact” and duplicated pseudogenes that harbor the same microRNA response elements. Other genes share the same set of microRNA response elements in the 3′ untranslated region of the transcripts and, consequently, will bind the same set of microRNAs. These genes form a network that, when transcribed, will influence the expression of all genes in the network. This relationship means that all the mRNA transcripts in the network can function as decoys. This recognition accounts for the functional utility of unitary pseudogenes.

One important consequence of this hypothesis is that mRNA has dual functions inside the cell. First, it encodes information needed to make proteins. Second, it helps regulate the expression of other transcripts that are part of its network.

Junk DNA and the Case for Creation

Evolutionary biologists have long maintained that identical (or nearly identical) pseudogene sequences found in corresponding locations in genomes of organisms that naturally group together (such as humans and the great apes) provide compelling evidence for shared ancestry. This interpretation was persuasive because molecular geneticists regarded pseudogenes as nonfunctional, junk DNA. Presumably, random biochemical events transformed functional DNA sequences (genes) into nonfunctional garbage.

Creationists and intelligent design proponents had little to offer by way of evidence for the intentional design of genomes. But all this changed with the discovery that virtually every class of junk DNA has function, including all three types of pseudogenes (processed, duplicated, and unitary).

If junk DNA is functional, then the sequences previously thought to show common descent could be understood as shared designs. The competitive endogenous RNA hypothesis supports this interpretation. This model provides an elegant rationale for the structural similarity between gene-pseudogene pairs and also makes sense of the widespread presence of unitary pseudogenes in genomes.

Of course, this insight also supports the RTB genomics model. And that sure feels good to me.

Resources

Endnotes
  1. Abdella M. Habib et al., “Microdeletion in a FAAH Pseudogene Identified in a Patient with High Anandamide Concentrations and Pain Insensitivity,” British Journal of Anaesthesia, advanced access publication, doi:10.1016/j.bja.2019.02.019.
  2. Ana C. Marques, Jennifer Tan, and Chris P. Ponting, “Wrangling for microRNAs Provokes Much Crosstalk,” Genome Biology 12, no. 11 (November 2011): 132, doi:10.1186/gb-2011-12-11-132; Leonardo Salmena et al., “A ceRNA Hypothesis: The Rosetta Stone of a Hidden RNA Language?”, Cell 146, no. 3 (August 5, 2011): 353–58, doi:10.1016/j.cell.2011.07.014.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/05/08/pseudogene-discovery-pains-evolutionary-paradigm

Why Mitochondria Make My List of Best Biological Designs

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BY FAZALE RANA – MAY 1, 2019

A few days ago, I ran across a BuzzFeed list that catalogs 24 of the most poorly designed things in our time. Some of the items that stood out from the list for me were:

  • serial-wired Christmas lights
  • economy airplane seats
  • clamshell packaging
  • juice cartons
  • motion sensor faucets
  • jewel CD packaging
  • umbrellas

What were people thinking when they designed these things? It’s difficult to argue with BuzzFeed’s list, though I bet you might add a few things of your own to their list of poor designs.

If biologists were to make a list of poorly designed things, many would probably include…everything in biology. Most life scientists are influenced by an evolutionary perspective. Thus, they view biological systems as inherently flawed vestiges cobbled together by a set of historically contingent mechanisms.

Yet as our understanding of biological systems improves, evidence shows that many “poorly designed” systems are actually exquisitely assembled. It also becomes evident that many biological designs reflect an impeccable logic that explains why these systems are the way they are. In other words, advances in biology reveal that it makes better sense to attribute biological systems to the work of a Mind, not to unguided evolution.

Based on recent insights by biochemist and origin-of-life researcher Nick Lane, I would add mitochondria to my list of well-designed biological systems. Lane argues that complex cells and, ultimately, multicellular organisms would be impossible if it weren’t for mitochondria.1(These organelles generate most of the ATP molecules used to power the operations of eukaryotic cells.) Toward this end, Lane has demonstrated that mitochondria’s properties are just-right for making complex eukaryotic cells possible. Without mitochondria, life would be limited to prokaryotic cells (bacteria and archaea).

To put it another way, Nick Lane has shown that prokaryotic cells could never evolve the complexity needed to form cells with complexity akin to the eukaryotic cells required for multicellular organisms. The reason has to do with bioenergetic constraints placed on prokaryotic cells. According to Lane, the advent of mitochondria allowed life to break free from these constraints, paving the way for complex life.

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Figure 1: A Mitochondrion. Image credit: Shutterstock

Through Lane’s discovery, mitochondria reveal exquisite design and logical architecture and operations. Yet this is not necessarily what I (or many others) would have expected if mitochondria were the result of evolution. Rather, we’d expect biological systems to appear haphazard and purposeless, just good enough for the organism to survive and nothing more.

To understand why I (and many evolutionary biologists) would hold this view about mitochondria and eukaryotic cells (assuming that they were the product of evolutionary processes), it is necessary to review the current evolutionary explanation for their origins.

The Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis is the best explanation for the origin of complex eukaryotic cells. This hypothesis states that complex cells originated when single-celled microbes formed symbiotic relationships. “Host” microbes (most likely archaea) engulfed other archaea and/or bacteria, which then existed inside the host as endosymbionts.

The presumption, then, is that organelles, including mitochondria, were once endosymbionts. Evolutionary biologists believe that, once engulfed, the endosymbionts took up permanent residency within the host cell and even grew and divided inside the host. Over time, the endosymbionts and the host became mutually interdependent. For example, the endosymbionts provided a metabolic benefit for the host cell, such as serving as a source of ATP. In turn, the host cell provided nutrients to the endosymbionts. The endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts’ genomes were transferred into the genome of the host organism.

Based on this scenario, there is no real rationale for the existence of mitochondria (and eukaryotic cells). They are the way they are because they just wound up that way.

But Nick Lane’s insights suggest otherwise.

Lane’s analysis identifies a deep-seated rationale that accounts for the features of mitochondria (and eukaryotic cells) related to their contribution to cellular bioenergetics. To understand why mitochondria and eukaryotic cells are the way they are, we first need to understand why prokaryotic cells can never evolve into large complex cells, a necessary step for the advent of complex multicellular organisms.

Bioenergetics Constraints on Prokaryotic Cells

Lane has discovered that bioenergetics constraints keep bacterial and archaeal cells trapped at their current size and complexity. Key to discovering this constraint is a metric Lane devised called Available Energy per Gene (AEG). It turns out that AEG in eukaryotic cells can be as much as 200,000 times larger than the AEG in prokaryotic cells. This extra energy allows eukaryotic cells to engage in a wide range of metabolic processes that support cellular complexity. Prokaryotic cells simply can’t afford such processes.

An average eukaryotic cell has between 20,000 to 40,000 genes; a typical bacterial cell has about 5,000 genes. Each gene encodes the information the cell’s machinery needs to make a distinct protein. And proteins are the workhorse molecules of the cell. More genes mean a more diverse suite of proteins, which means greater biochemical complexity.

So, what is so special about eukaryotic cells? Why don’t prokaryotic cells have the same AEG? Why do eukaryotic cells have an expanded repertoire of genes and prokaryotic cells don’t?

In short, the answer is: mitochondria.

On average, the volume of eukaryotic cells is about 15,000 times larger than that of prokaryotic cells. Eukaryotic cells’ larger size allows for their greater complexity. Lane estimates that for a prokaryotic cell to scale up to this volume, its radius would need to increase 25-fold and its surface area 625-fold.

Because the plasma membrane of bacteria is the site for ATP synthesis, increases in the surface area would allow the hypothetically enlarged bacteria to produce 625 times more ATP. But this increased ATP production doesn’t increase the AEG. Why is that?

The bacteria would have to produce 625 times more proteins to support the increased ATP production. Because the cell’s machinery must access the bacteria’s DNA to make these proteins, a single copy of the genome is insufficient to support all of the activity centered around the synthesis of that many proteins. In fact, Lane estimates that for bacteria to increase its ATP production 625-fold, it would require 625 copies of its genome. In other words, even though the bacteria increased in size, in effect, the AEG remains unchanged.

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Figure 2: ATP Production at the Cell Membrane Surface. Image credit: Shutterstock

Things become more complicated when factoring in cell volume. When the surface area (and concomitant ATP production) increase by a factor of 625, the volume of the cell expands 15,000 times. To satisfy the demands of a larger cell, even more copies of the genome would be required, perhaps as many as 15,000. But energy production tops off at a 625-fold increase. This mismatch means that the AEG drops by 25 percent per gene. For a genome consisting of 5,000 genes, this drop means that a bacterium the size of a eukaryotic cell would have about 125,000 times less AEG than a typical eukaryotic cell and 200,000 times less AEG when compared to eukaryotes with genome sizes approaching 40,000 genes.

Bioenergetic Freedom for Eukaryotic Cells

Thanks to mitochondria, eukaryotic cells are free from the bioenergetic constraints that ensnare prokaryotic cells. Mitochondria generate the same amount of ATP as a bacterial cell. However, their genome consists of only 13 proteins, thus the organelle’s ATP demand is low. The net effect is that the mitochondria’s AEG skyrockets. Furthermore, mitochondrial membranes come equipped with an ATP transport protein that can pump the vast excess of ATP from the organelle interior into the cytoplasm for the eukaryotic cell to use.

To summarize, mitochondria’s small genome plus its prodigious ATP output are the keys to eukaryotic cells’ large AEG.

Of course, this raises a question: Why do mitochondria have genomes at all? Well, as it turns out, mitochondria need genomes for several reasons (which I’ve detailed in previous articles).

Other features of mitochondria are also essential for ATP production. For example, cardiolipinin the organelle’s inner membrane plays a role in stabilizing and organizing specific proteinsneeded for cellular energy production.

From a creation perspective it seems that if a Creator was going to design a eukaryotic cell from scratch, he would have to create an organelle just like a mitochondrion to provide the energy needed to sustain the cell’s complexity with a high AEG. Far from being an evolutionary “kludge job,” mitochondria appear to be an elegantly designed feature of eukaryotic cells with a just-right set of properties that allow for the cellular complexity needed to sustain complex multicellular life. It is eerie to think that unguided evolutionary events just happened to traverse the just-right evolutionary path to yield such an organelle.

As a Christian, I see the rationale that undergirds the design of mitochondria as the signature of the Creator’s handiwork in biology. I also view the anthropic coincidence associated with the origin of eukaryotic cells as reason to believe that life’s history has purpose and meaning, pointing toward the advent of complex life and humanity.

So, now you know why mitochondria make my list.

Resources

Endnotes
  1. Nick Lane, “Bioenergetic Constraints on the Evolution of Complex Life,” Cold Spring Harbor Perspectives in Biology 6, no. 5 (May 2014): a015982, doi:10.1101/cshperspect.a015982.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/05/01/why-mitochondria-make-my-list-of-best-biological-designs